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Herein, we sought to examine the potential regulation of HDAC6 in cardiac remodelling post\u2010infarction. Experimental myocardial infarction (MI) was created in HDAC6\u2010deficient (HDAC6<jats:sup>\u2212\/\u2212<\/jats:sup>) mice and wild\u2010type (HADC6<jats:sup>+\/+<\/jats:sup>) by left coronary artery ligation. At days 0 and 14 post\u2010MI, we evaluated cardiac function, morphology and molecular endpoints of repair and remodelling. At day 14 after surgery, the ischemic myocardium had increased levels of HADC6 gene and protein of post\u2010MI mice compared to the non\u2010ischemic myocardium of control mice. As compared with HDAC6<jats:sup>\u2212\/\u2212<\/jats:sup>\u2010MI mice, HADC6 deletion markedly improved infarct size and cardiac fibrosis as well as impaired left ventricular ejection fraction and left ventricular fraction shortening. At the molecular levels, HDAC6<jats:sup>\u2212\/\u2212<\/jats:sup> resulted in a significant reduction in the levels of the transforming growth factor\u2010beta 1 (TGF\u2010\u03b21), phosphor\u2010Smad\u20102\/3, collagen I and collagen III proteins and\/or in the ischemic cardiac tissues. All of these beneficial effects were reproduced by a pharmacological inhibition of HADC6 in\u00a0vivo. In\u00a0vitro, hypoxic stress increased the expressions of HADC6 and collagen I and III gene; these alterations were significantly prevented by the HADC6 silencing and TubA loading. These findings indicated that HADC6 deficiency resists ischemic injury by a reduction of TGF\u2010\u03b21\/Smad2\/3 signalling activation, leading to decreased extracellular matrix production, which reduces cardiac fibrosis and dysfunction, providing a potential molecular target in the treatment of patients with MI.<\/jats:p>","DOI":"10.1111\/jcmm.70063","type":"journal-article","created":{"date-parts":[[2024,9,5]],"date-time":"2024-09-05T03:40:12Z","timestamp":1725507612000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Histone deacetylase 6 controls cardiac fibrosis and remodelling through the modulation of <scp>TGF<\/scp>\u2010\u03b21\/Smad2\/3 signalling in post\u2010infarction mice"],"prefix":"10.1111","volume":"28","author":[{"given":"Junqiao","family":"Fang","sequence":"first","affiliation":[{"name":"Department of Cardiology and Hypertension, Jilin Provincial Key Laboratory of Stress and Cardiovascular 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